Upregulation of ceramide via the de novo pathway and the hydrolysis of sphingomyelin by GT3 in pancreatic cancer cells regardless of their Ras status. Previous studies had shown that apoptosis is induced by GT3 in both wild type and mutated K-Ras pancreatic cancer cell lines via a mechanism that involves disruption of signaling of receptor tyrosine kinase ErbB2. This evidence concerns the gene KRAS and familial pancreatic carcinoma.